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  • Title: Calcium-dependent control of volume regulation in renal proximal tubule cells: I. Swelling-activated Ca2+ entry and release.
    Author: McCarty NA, O'Neil RG.
    Journal: J Membr Biol; 1991 Aug; 123(2):149-60. PubMed ID: 1659640.
    Abstract:
    The mechanism of Ca(2+)-dependent control of hypotonic cell volume regulation was investigated in the isolated, nonperfused renal proximal straight tubule. When proximal tubules were exposed to hypotonic solution with 1 mM Ca2+, cells swelled rapidly and then underwent regulatory volume decrease (RVD). This treatment resulted in an increase in intracellular free calcium concentration ([Ca2+]i) by a mechanism that had two phases: the first was a transient increase from baseline (136 nM) to a peak (413 nM) that occurred in the first 15-20 sec, but was followed by a rapid decay toward the pre-swelling levels. The second phase was characterized by a sustained elevation of [Ca2+]i above the baseline (269 nM), which was maintained over several minutes. The dependence of these two phases on extracellular Ca2+ was determined. Reduction of bath [Ca2+] to 10 or 1 microM partially diminished the transient phase, but abolished the sustained phase completely, such that [Ca2+]i fell below the baseline levels during RVD. It was concluded that the transient increase resulted predominantly from swelling-activated release of intracellular Ca2+ stores and that the sustained phase was due to swelling-activated Ca2+ entry across the plasma membrane. Ca2+ entry probably also contributed to the transient increase in [Ca2+]i. The time dependence of swelling-activated Ca2+ entry was also investigated, since it was previously shown that RVD was characterized by a "calcium window" period (less than 60 sec), during which extracellular Ca2+ was required. Outside of this time period, RVD would inactivate and could not be reactivated by subsequent addition of Ca2+. It was found that the Ca2+ permeability did not inactivate over several minutes, indicating that the temporal dependence of RVD on extracellular Ca2+ is not due to the transient activation of a Ca2+ entry pathway.
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